Natural History of Early, Localized Prostate Cancer: A Final Report from Three Decades of Follow-up

Popiołek, Marcin; Rider, Jennifer R.; Andrén, Ove; Andersson, Sven‐Olof; Holmberg, Lars; Adami, Hans‐Olov; Johansson, Jan‐Erik

doi:10.1016/j.eururo.2012.10.002

Cited by 198 publications

(133 citation statements)

References 18 publications

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“…A straightforward example is provided by docetaxel and cabazitaxel, the only two "cytotoxic" agents approved in prostate cancer (13,14). Given the often very indolent nature of prostate cancer, it is difficult to argue that mitotic arrest is the mechanism of action for docetaxel and cabazitaxel in this disease (15)(16)(17). Instead, it is increasingly accepted that interference with trafficking of the androgen receptor is the mechanism of action (18,19), a concept reinforced by the demonstration of tumors previously thought to be "androgen independent" that in fact continue to be very dependent on androgens (20)(21)(22).…”

Section: Discussionmentioning

confidence: 99%

Microtubule-targeting agents augment the toxicity of DNA-damaging agents by disrupting intracellular trafficking of DNA repair proteins

Poruchynsky

Komlódi-Pásztor

Trostel

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

152

115

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The paradigm that microtubule-targeting agents (MTAs) cause cell death via mitotic arrest applies to rapidly dividing cells but cannot explain MTA activity in slowly growing human cancers. Many preferred cancer regimens combine a MTA with a DNA-damaging agent (DDA). We hypothesized that MTAs synergize with DDAs by interfering with trafficking of DNA repair proteins on interphase microtubules. We investigated nine proteins involved in DNA repair: ATM, ATR, DNA-PK, Rad50, Mre11, p95/NBS1, p53, 53BP1, and p63. The proteins were sequestered in the cytoplasm by vincristine and paclitaxel but not by an aurora kinase inhibitor, colocalized with tubulin by confocal microscopy and coimmunoprecipitated with the microtubule motor dynein. Furthermore, adding MTAs to radiation, doxorubicin, or etoposide led to more sustained γ-H2AX levels. We conclude DNA damage-repair proteins traffic on microtubules and addition of MTAs sequesters them in the cytoplasm, explaining why MTA/DDA combinations are common anticancer regimens.

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Section: Discussionmentioning

confidence: 99%

Microtubule-targeting agents augment the toxicity of DNA-damaging agents by disrupting intracellular trafficking of DNA repair proteins

Poruchynsky

Komlódi-Pásztor

Trostel

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

152

115

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“…No association with very high intake of lycopene 3 Defined as T3-T4, or Gleason score 8-10, or nodal involvement. 4 Adjusted for age at diagnosis, race, calendar year of diagnosis, tumor extent, nodal involvement, Gleason score, history of prediagnosis prostatespecific antigen testing, education, physical activity, BMI, smoking, multivitamin supplement use, and fish intake. 5 Prediagnosis dietary intake was based on 1992 questionnaire.…”

Section: Resultsmentioning

confidence: 99%

“…In overall analyses, 3 Defined as T3-T4, or Gleason score 8-10, or nodal involvement. 4 Adjusted for age at diagnosis, race, calendar year of diagnosis, tumor extent, nodal involvement, Gleason score, history of prediagnosis prostatespecific antigen testing, education, initial treatment, history of cardiovascular disease, physical activity, smoking status and total dairy intake. 5 The ranges of lycopene intake for quartiles 1-4 in 1999 were <3.1, 3.12<4.4, 4.42<6.2, 6.2-40.9 mg/day, and in 2003 were <3.2, 3.22<4.5, 4.52<6.3, 6.3-43.0 mg/day.…”

Section: Resultsmentioning

confidence: 99%

“…3 Although localized prostate cancer is mostly indolent, local progression and distant metastasis can develop over the long term and cause prostate cancer death. 4 In addition, men with high-grade tumors (Gleason score [8][9][10] are at least four times as likely to die from prostate cancer as men with low-grade tumors (Gleason score 2-6). 5 Although data are still limited, a growing number of studies suggest that longterm postdiagnosis diet plays a role in prostate cancer progression and eventually prostate cancer mortality.…”

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confidence: 99%

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Lycopene, tomato products and prostate cancer‐specific mortality among men diagnosed with nonmetastatic prostate cancer in the Cancer Prevention Study II Nutrition Cohort

Wáng

Jacobs

Newton

et al. 2016

Intl Journal of Cancer

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While dietary lycopene and tomato products have been inversely associated with prostate cancer incidence, there is limited evidence for an association between consumption of lycopene and tomato products and prostate-cancer specific mortality (PCSM). We examined the associations of prediagnosis and postdiagnosis dietary lycopene and tomato product intake with PCSM in a large prospective cohort. This analysis included men diagnosed with nonmetastatic prostate cancer between enrollment in the Cancer Prevention Study II Nutrition Cohort in 1992 or 1993 and June 2011. Prediagnosis dietary data, collected at baseline, were available for 8,898 men, of whom 526 died of prostate cancer through 2012. Postdiagnosis dietary data, collected on follow-up surveys in 1999 and/or 2003, were available for 5,643 men, of whom 363 died of prostate cancer through 2012. Cox proportional hazards regression was used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs) for PCSM. Neither prediagnosis nor postdiagnosis dietary lycopene intake was associated with PCSM (fourth vs. first quartile HR 5 1.00, 95% CI 0.78-1.28; HR 5 1.22, 95% CI 0.91-1.64, respectively). Similarly, neither prediagnosis nor postdiagnosis consumption of tomato products was associated with PCSM. Among men with high-risk cancers (T3-T4 or Gleason score 8-10, or nodal involvement), consistently reporting lycopene intake median on both postdiagnosis surveys was associated with lower PCSM (HR 5 0.41, 95% CI 0.17-0.99, based on ten PCSM cases consistently median intake) compared to consistently reporting intake < median. Future studies are needed to confirm the potential inverse association of consistently high lycopene intake with PCSM among men with high-risk prostate cancers.Prostate cancer is the most commonly diagnosed cancer, and the second leading cause of cancer death among men in the United States. 1 There are nearly 3 million prostate cancer survivors currently living in the United States, accounting for 20% of all cancer survivors, and the number is still increasing with 220,000 new cases diagnosed each year. 2 Despite a generally good prognosis, death from prostate cancer, even for men diagnosed with localized prostate cancer, is still a concern. 3 Although localized prostate cancer is mostly indolent, local progression and distant metastasis can develop over the long term and cause prostate cancer death. 4 In addition, men with high-grade tumors (Gleason score 8-10) are at least four times as likely to die from prostate cancer as men with low-grade tumors (Gleason score 2-6). 5 Although data are still limited, a growing number of studies suggest that longterm postdiagnosis diet plays a role in prostate cancer progression and eventually prostate cancer mortality. [6][7][8][9] Lycopene, found predominantly in tomato products, is a major carotenoid widely distributed in the human body. Lycopene accumulates in several key organs including the prostate gland. 10 Lycopene is hypothesized to have anticarcinogenic effects primarily due to its antioxi...

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“…Many studies have described several aspects of the natural history and long-term survival in prostate cancer, in both observational and randomised controlled trials (RCT) [1][2][3]. Continual evaluation and analyses of PCa survival is vital if we are to ensure that effectiveness in management of the disease is maintained and improved as far as possible.…”

Section: Introductionmentioning

confidence: 99%

Disease-Specific Survival in Prostate Cancer Patients : Results from the Scandinavian Prostate Cancer Group (SPCG) Trial No. 5 and Regional Cancer Register Data

Klaff¹

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Introduction Prostate cancer (PCa) is the most common cancer among men in Sweden. The clinical course varies considerably, which makes it difficult to predict the prognosis in the individual case. In order to explore the early as well as the late course of the disease, large study groups and population-based cohorts are necessary. Aims To explore factors that influence the long-term outcome of men with low-risk tumours in a population-based register, to predict the long-term course, and to assess the mortality rate for men with prostate cancer (Paper I) To analyse long-term outcome and to investigate factors associated with long-term survival in patients with metastases to the skeleton (Paper II) To analyse early androgen deprivation treatment (ADT) failure and to define clinical predictors associated with short survival due to early ADT failure in prostate cancer patients with bone metastases (Paper III) To analyse the prognostic significance of the extent of bone metastases in relation to other pretreatment variables in prostate cancer patients, and to explore the impact of bone metastases on quality-of-life (Paper IV) Material and methods The study groups were assembled from The South East Region Prostate Cancer Register (SERPCR), and The Scandinavian Prostate Cancer Group (SPCG) Trial No. 5. In the first study, prognostic factors and long-term disease-specific mortality rates of low-risk prostate cancer patients from the early PSA era were analysed. In the second study, patient-related factors, quality-of-life (QoL) and long-term survival in 915 PCa patients with bone metastases (M1b) under ADT, were analysed. In Study III factors predicting primary failure to respond to ADT were identified. Study IV explored the impact of the extent of bone metastases on survival and QoL for these men. Result and conclusions The long-term disease-specific mortality of low-risk localised PCa is low, but the annual mortality rate gradually increases. This indicates that some tumours slowly develop into lethal cancer, particularly in men 70 years or older and with a PSA level ≥ 4 μg/L. From the SPCG Trial No. 5, a subgroup of patients with M1b disease and favourable set of predictive factors survived more than 10 years under ADT with an acceptable QoL. Independent predictors of long-term survival were identified as performance status (PS) < 2, limited extent of bone metastases, and a PSA level < 231 μg/L at the time of enrolment in the trial. However, four independent clinical predictors of early ADT failure could be defined. Men exhibiting these features should be considered for an alternative treatment. Patient grouping based on three categories of extent of bone metastases related to PS, haemoglobin, and QoL at presentation, as independent predictors of mortality, may provide improved accuracy of prognosis

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Natural History of Early, Localized Prostate Cancer: A Final Report from Three Decades of Follow-up

Cited by 198 publications

References 18 publications

Microtubule-targeting agents augment the toxicity of DNA-damaging agents by disrupting intracellular trafficking of DNA repair proteins

Microtubule-targeting agents augment the toxicity of DNA-damaging agents by disrupting intracellular trafficking of DNA repair proteins

Lycopene, tomato products and prostate cancer‐specific mortality among men diagnosed with nonmetastatic prostate cancer in the Cancer Prevention Study II Nutrition Cohort

Disease-Specific Survival in Prostate Cancer Patients : Results from the Scandinavian Prostate Cancer Group (SPCG) Trial No. 5 and Regional Cancer Register Data

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